Citations

To study the separate actions of peripheral and central temperature-sensitive systems on the cutaneous veins of the dog, a cross-circulation preparation was made in which hindleg and central temperatures could be varied independently. The lateral saphenous vein of a vascularly isolated hindleg was cross-perfused at constant flow; the difference between perfusion and femoral vein pressures was a measure of venomotor activity. With central temperature constant, local cooling of one leg from 47° to 17°C caused the lateral saphenous vein to constrict; sensitivity to cooling was maximal between 42° and 27°C. With leg temperature constant, central cooling caused the lateral saphenous vein to constrict; over the range of 40° to 33°C, the constriction was linearly related to the decrease in temperature. Central heating reduced the response to local cooling, whereas central cooling had the opposite effect. Thus a decrease in central temperature from 38° to 34°C increased the venoconstrictor response to local cooling from 42° to 22°C by a factor of ten or more.

In 13 canine hearts, 158 disappearance curves for 133 Xe and antipyrine-1 125 I, given by intra-arterial slug injection, were recorded at a wide range of perfusion rates. Flow rates (ml/100 g/min) calculated from these curves by a variety of methods were compared with measured flow rates (F a ) per weight of perfused tissue. Perfusion of isolated, supported hearts and of anterior descending coronary arteries in open-chest dogs provided similar data. The semilogarithmic slope of curves from apex or whole heart decreased with time, particularly at high flow rates. There was a small, consistent difference in shape between antipyrine and xenon curves, suggesting that radioactivity in fat contributed somewhat to this tailing. Estimation of flow rate from the steepest semilog slope yielded an average value of 1.1 F a for all rates; estimation from slope at 30% of peak radioactivity gave 0.9F a . The curves were closely described by a two-exponential equation which gave flow estimates of 0.95F a when collimation limited the observations to the heart apex, and lower values when the whole heart was observed. Peak height/area methods gave values of approximately 0.75F a in spite of various compensations for the impossibility of recording the curve until radioactivity = 0.

Multiple measurements of left ventricular volumes, ejection fractions, and circulatory pressures were made under conditions of varied outflow resistance in five intact anesthetized dogs by using a biplane videoangiographic recording system which displays simultaneously two roentgen images on the same television screen, records the images on video tape, and requires low radiation levels and small amounts of contrast medium. Aortic pressure was controlled by intra-aortic infusion of angiotensin or acetylcholine. With spontaneous sinus rhythm and normal aortic pressure, end-diastolic volume averaged 35 ml (2.3 ml/kg), and ejection fraction averaged 47% of end-diastolic volume. When aortic pressure was increased, average end-diastolic volumes increased to 53 ml and ejection fractions decreased to 29%. Conversely, when aortic pressure was decreased, average ejection fraction increased to 73%, although changes in stroke volume were usually not large under these conditions. Concomitant large changes in the shape of the left ventricular cavity were also observed. Similar changes were observed when heart rate was maintained constant by electrical pacing of the atria and ventricles with a constant atrial-ventricular stimulus interval. The variability in left ventricular volume and ejection fraction observed in the same animal during different circulatory states may account in part for the differences in values for these variables reported by different investigators.

The effect of exercise on the vasoconstrictive response to sympathetic stimulation was studied by observing the changes in perfusion pressure in dogs' hindlimbs perfused at constant flow. During steady-state simulated exercise, a time-dependent increase occurred between 10 and 30 minutes in the magnitude of response to lumbar trunk stimulation or carotid sinus hypotension. This was present (although to a reduced Degrees) in drug-induced vasodilatation and in exercising limbs perfused at constant pressure. The time-dependent change was not due to (1) repetition of stimulus, (2) artifact from muscle electrodes, (3) circulating vasoactive substances, (4) skin circulation, or (5) pH, P CO 2 , or temperature of the perfusing blood. When norepinephrine was used as the vasoconstrictive stimulus, no time-dependent change was noted. After stabilization, the frequency-response curve of exercising muscle exceeded that at rest at all blood concentrations of norepinephrine and at all save the lowest frequencies of stimulation. It was concluded that vascular smooth muscle can develop greater tension from greater initial length. However, during exercise some factor which operates between the sympathetic nerve ending and the receptor site on vascular smooth muscle initially tends to depress this enhanced ability to develop tension.

The lateral saphenous vein of the dog was perfused with homologous blood at constant, flow. Changes in perfusion pressure were used to measure active changes in venous tone. Cooling of the perfusate caused the vein to constrict and warming to relax. Most of the change occurred over the temperature range of 27° to 42°C. The powerful venoconstrictor response to cooling depended on intact sympathetic nerves, since it was reduced by lumbar sympathectomy and largely abolished by alpha-receptor or ganglionic blockade. The response was confined to the vein being cooled. By comparison, cooling the body core when the temperature of the blood in the vein was 37°C caused a generalized constriction of the superficial limb veins. These responses were impaired by anesthetic agents (for example, pentobarbital), by generalized hypoxia, and by arterial hypotension. The data indicate a role for the cutaneous veins in temperature regulation. In the cold, the venous return is directed preferentially to the venae comitantes for heat preservation through countercurrent exchange with the arteries, and in warmth to the superficial veins for heat dissipation.

Isolated cat lungs perfused at constant flow (75 ml/min per kg total body weight) were ventilated with gases of varying CO 2 content (0 to 10%), 20% O 2 , and the balance N 2 . Tidal volume was constant, and airway pressure did not change. Left atrial pressure was held constant, and changes in pulmonary artery pressure (PPA) were taken to reflect changes in pulmonary vascular resistance. Progressive hypercapnia (Pco 2 = 0 to 60 mm Hg) resulted in an increase in PPA as pH decreased. Equivalent degrees of acidosis, produced by the infusion of 0.3 N lactic acid, resulted in a higher PPA. Changes in PPA produced by lactic acid were reversible with 0.89 M sodium bicarbonate. With Pco 2 constant, and pH changed by lactic acid or sodium bicarbonate infusion, PPA was higher in lungs ventilated with room air (Pco 2 = 0) than in those ventilated with 5 or 10% CO 2 (Pco 2 = 30 or 60 mm Hg) at the same hydrogen ion concentration of the perfusate. These findings can be explained by two opposing actions of CO 2 on pulmonary vessels: a dilator action due to the direct effect of CO 2 and a constrictor action caused by the increase in hydrogen ion concentration.

A field study was made of the effect of β-adrenergic receptor blockade (propranolol; Kö 592) on the racing performance of six normal greyhounds and three with chronic extrinsic cardiac denervation. Records were made of the time to race a 5/16-mile course before and after blockade; the heart rate was recorded by telemetry. After the administration of the β-adrenergic receptor-blocking agent to the normal greyhound, racing time was slightly increased, and maximal heart rate was slighdy decreased. After blockade in the cardiac denervated greyhounds, racing time was prolonged, cardiac acceleration was severely limited, and the animals finished running in a state of collapse. The data indicated diat die cardiostimulant action of both sympathetic nerves and circulating catecholamines was necessary for maximal performance. After blockade of one or the other of these mechanisms, racing performance was slightly reduced from normal. Withdrawal of both adjuvants severely limited the performance of maximal exercise.

Cardiac and aortic pressures were recorded after stellate ganglionectomy and vagotomy. Acute heart block was produced by injecting the atrioventricular node, and atrial and ventricular systoles were controlled electronically to occur independently or in any desired relationship. Angiocardiograms recorded on video tape after injections of 4 ml 69% Renovist into the left ventricle were analyzed with a videodensitometer able to detect small refluxes of contrast medium into the left atrium and correlate them with phases of the cardiac cycle. When ventricular driving was temporarily suspended but atrial driving continued, pressure records indicated mitral valve closure after each atrial systole, but reflux of contrast medium into the atrium occurred after each systole not followed by a normally sequenced ventricular systole. Driving with a 2: 1 atrioventricular stimulation resulted in reflux, with the alternate atrial contraction dissociated from ventricular systole. Thus, the mitral valve was not effectively closed by atrial systoles that were not followed by normally sequenced ventricular systoles.

Intrapericardial pressures were recorded via a saline-filled Teflon catheter (o. d., 1.3 mm) in 11 anesthetized dogs studied without thoracotomy. Seven animals were studied before, during, and after 1-min exposures to transverse accelerations that ranged from 1G (normal gravitational environment) to 7G when in the supine (+G j ), prone (-G x ), left decubitus (+G v ), and right decubitus (-G y ) positions. Four additional animals were studied at 1G only, while in these same body positions. Pressures also were recorded from both atria, right ventricle, aorta, esophagus, and the potential pleural space. Mean end-expiratory intrapericardial pressure varied directly with the vertical height of the recording site in the thorax during all conditions studied, as would be expected in a hydrostatic system. Transpericardial pressures were not significantly different from zero at all levels of acceleration studied. Transmural left and right atrial pressures were independent of the height of the recording site in the thorax and were unchanged during exposures to transverse accelerations that ranged from plus to minus 7G x .

Pressures at multiple sites in the thorax of supine anesthetized dogs were recorded simultaneously with fluid-filled catheters inserted percutaneously. Pleural and pericardial pressures were corrected to the level of their respective recording catheter tips as determined by roentgenograms. Intracardiac pressures were referred to the midthoracic coronal plane or to the vertical level of the pericardial catheter tip. Pericardial pressures at end-expiration averaged -5.0 cm H 2 O (range 0 to - 13) and varied with the vertical position of the catheter tip, becoming less negative as the height above the midthoracic coronal plane diminished. Acute right heart failure was produced by partial obstruction of the pulmonary artery by a catheter-tip balloon. Although mean right atrial pressure increased by an average of 26 cm H 2 O, consistent increases in pericardial pressure did not occur. Similarly, during acute obstruction to left ventricular outflow by inflation of a balloon within the thoracic aorta, left atrial end-diastolic pressure increased by an average of 14.5 cm H 2 O, but no consistent increase in pericardial pressure was recorded. No systematic changes in pleural pressure were detected in either case. Thus there was no evidence of pericardial restriction of cardiac dilatation during acute heart failure under these experimental conditions.